Separation paradigms in monkeys have proved to be valuable animal models of human loss-related affective disturbance. Until the present, the most reliable separation-induced affective behavioral changes have occurred in young monkey subjects, using mother-infant or peer separation paradigms. Recently, however, we observed an adult female Macaca nemestrina monkey who developed an affective behavioral disturbance responsive to a tricyclic antidepressent following several losses. This animal's vulnerability to depression following loss was subsequently demonstrated experimentally (Rasmussen and Reite 1982). The results of this study, as well as observations on several other adult females in the Primate Laboratory who had shown an apparent loss-related affective disturbance, suggested that a high degree of psychosocial stress (and concomitant physiological status) might have been a factor in predisposing those animals to react especially severely to loss. We propose to document the behavioral response of 10 adult pigtailed macaques (M. nemestrina) to separation from significant others in the context of their social group. Since differences in automatic reactivity have been shown to be predictive of the severity of behavioral response to separation in infant monkeys (Suomi et al. 1981), we will also test the heart rate reactivity of or adult subjects prior to separation. If the apparent vulnerability of certain adult animals to loss-induced behavioral depression can be substantiated in a controlled prospective experiment, this would significantly enhance the usefulness of primate separation models of depression, since we believe that models of depression in adult monkeys would bear a closer resemblance to affective disorders in adult humans. The identification of environmental factors (social stress) and physiological factors (autonomic reactivity) which may be predictive of the severity of the adult macaque's affective behavioral response to separation may have important implications for our understanding of etiological mechanisms involved in human affective disorders.